Titanium Dioxide Nanoparticles Trigger Loss of Hepatic Function and Perturbation of Mitochondrial Dy-资料下载-美国布鲁克海文仪器公司

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阅读：257 发布时间：2015-6-2

Titanium dioxide (TiO2) nanoparticles are one of the most highly manufactured

nanomaterials in the world with applications in copious industrial and consumer products.

The liver is a major accumulation site for many nanoparticles, including TiO2, directly

through intentional ingestion or indirectly through increased environmental contamination

and unintentional ingestion via water, food or animals. Growing concerns over the current

usage of TiO2 coupled with the lack of mechanistic understanding of its potential health

risk is the motivation for this study. Here we determined the toxic effect of three different

TiO2 nanoparticles (commercially available rutile, anatase and P25) on primary rat

hepatocytes. Specifically, we evaluated events related to hepatic functions and

mitochondrial dynamics: (1) urea and albumin synthesis using colorimetric and ELISA

assays, respectively; (2) redox signaling mechanisms by measuring ROS production; (3)

OPA1 and Mfn-1 expression that mediates the mitochondria dynamics by PCR; and (4)

mitochondrial morphology by MitoTracker Green FM staining. All three TiO2

nanoparticles induced a significant loss in hepatic functions even at concentrations as low

as 20 μg/ml with commercially used P25 causing maximum damage. TiO2 nanoparticles

induced a strong oxidative stress in primary hepatocytes.TiO2 nanoparticles exposure also

resulted in morphological changes in mitochondria and significant loss in the fusion

process, thus impairing the mitochondrial dynamics. Although this study demonstrated that

TiO2 nanoparticles exposure resulted in significant damage in primary hepatocytes, more

in vitro and in vivo studies are required to determine the complete toxicological mechanism

on primary hepatocytes and subsequently liver function.